Tumor suppressor protein p53 and association of its gene TP53 with schizophrenia patients

The TP53 tumor suppressor gene guides synthesis of a tumor protein called p53 by encoding a phosphoprotein, which is a key element in maintaining genomic stability and cellular apoptosis. This protein functions as a tumor suppressor thereby, preventing cell growth in an uncontrolled way. The current paper provides insights in the favor of increased apoptosis, causing, neurodevelopmental abnormalities as well as schizophrenia-related tumor resistance. With the developments of reduced risk of cancer in patients with schizophrenia, this review is focused on the evidence about the association of TP53 with neurodevelopment. TP53 is a gene that can suppress the tumor causing Neuropraxia. The reduced expression of the oligodendrocyte/myelination genes and apoptotic processes in schizophrenia; abnormalities in white matter (WM), and integrity in schizophrenia suggest that major apoptosis regulators are interested in certain features of myelin integrity in schizophrenia. Neural apoptosis is believed to involve the tumor suppressor gene TP53. In the dopamine receptor D4 (DRD4), polymorphism at codon 72 is reported in TP53 with the long-form variants of the upstream variable number of tandem repeats (uVNTR). The protein p53, coded by the TP53 gene, plays a key role in apoptosis control and contributes to the development of oligodendrocytes. The variability of WM, metabolic activity, biochemistry markers, and membrane turnover can be accounted for by TP53 gene polymorphisms.